Lead Nephropathy: Revisiting an Overlooked Cause of Kidney Disease

Abstract

Despite the recognition of lead nephropathy as a consequence of environmental and occupational lead exposure, lead nephropathy still appears to be underrecognized by physicians as a cause and promoter of chronic kidney disease (CKD), especially in people with more apparent causative factors such as diabetes and hypertension. This review focuses on the clinical, pathophysiological and epidemiological perspectives of lead nephropathy with the objective of promoting the awareness of this important but overlooked cause of CKD among physicians. Literature was reviewed using available medical journals and online literature search through Google, Pubmed, Medline, Medscape and HINARI databases. The key words employed were: Lead Nephropathy, Environmental and Occupational lead exposure and chronic kidney disease. Lead nephropathy which is a tubulointerstitial nephritis, may present acutely or chronically in association with hypertension. The clinical diagnosis of lead nephropathy is complex, because the symptoms are varied and non-specific especially with subclinical nephrotoxicity. The recognition of lead nephropathy can be enhanced if physicians have a high index of suspicion in the assessment of patients with renal disease. It is recommended that the evaluation of environmental and occupational nephrotoxins like lead be incorporated into programs for the prevention of CKD, especially in developing countries where lead exposure and toxicity still remain largely unchecked and the prevalence and burden of CKD is increasing

An Evaluation of the Mitigating Effects of Α-Tocopherol (Vitamin E) and Ascorbic Acid (Vitamin C) on the Renal Function and Histology of Adult Male Albino Wistar Rats with Sub-Acute Lead Acetate Exposure

“…In addition other factors like the varying dose of lead used in the studies and the diverse level of lead exposure from acute, sub-acute and chronic may also account for the differences as the study duration in the work of Al-Attar et al [26] was 7 weeks, 10 weeks for the study by Salem et al [25], acute low level exposure for below 2 weeks by Ishiak et al [28], 1 week by Andjelkovic et al [27] and chronic low exposure of 3 months by Odigie et al [29]. In addition the differing results could also be explained by the recognition that serum urea and creatinine are less reliable markers of lead induced kidney damage as indicated by other reports [30] [31] [32] and the sample size limitations due to the ethical limitations for large animal sample population.…”

Detection of Lead (II) on a Boron-doped Diamond Electrode by Differential Pulse Anodic Stripping Voltammetry

“…However, lead has detrimental effects on the central nervous system of the developing infant [4,5]. Although neurotoxicity has the most sensitive endpoint, lead can also cause blood pressure, affect kidney function, cause mutagenesis and have reproductive effects [6]. Due to its toxicity, lead must be quantified in aqueous media with a view to controlling its use in several areas of human activity.…”

Assessment of heavy metals and potential health risks associated with the consumption of vegetables grown on the roadside soils

“…It has been found that Pb exposure increased the excretion of amino acids and glucose in urine due to its toxic effect on the proximal convoluted portion of the nephron (Loghman-Adham, 1997). Long-term Pb exposure causes kidney failure, increased blood uric acid concentration, high blood pressure, and joint infection (Alasia, 2010). The highest amounts of Pb (about 1/3rd of the entire body) were accumulated in the liver (Mudipalli, 2009).…”